Search

Type I interferons (IFN‐I) link innate to adaptive immunity in microbial infection, autoimmune disease and tumor immunity. It is not known whether IFN‐I have an equally central role in alloimmunity. Here we tested this possibility by studying skin allograft survival and donor‐specific CD8+T‐cell responses in mice that lack the IFN‐I receptor (IFN‐IR−/−). We found that IFN‐IR−/−mice reject fully allogeneic wild‐type skin grafts at the same rate as wild‐type recipients. Similarly, allograft rejection was not delayed if IFN‐IR−/−male skin was transplanted to syngeneic IFN‐IR−/−female mice. Quantitation of the male (H‐Y)‐specific CD8+T‐cell response in these mice revealed normal generation of donor‐specific CD8+effector T cells but fourfold reduction in CD8+memory T cells. Memory CD8+T cells generated in the absence of IFN‐IR had normal phenotype and recall function, assessed by ex vivo cytokine production and the ability of IFN‐IR−/−mice to mount second set rejection. Finally, these memory T cells were maintained at a constant number despite their inability to respond to IFN‐1. Our findings indicate that IFN‐I cytokines are not critical for acute allograft rejection or for the expansion and differentiation of donor‐specific CD8+T cells into long‐lived, functional memory T cells.

Using a reverse transcriptase-polymerase chain reaction method, a cDNA for the complete coding region and part of the 5′-untranslated region of rat IL-13 was cloned from rat renal cortex RNA following the induction of anti-glomerular basement membrane antibody-induced glomerulonephritis. The coding region of IL-13 cDNA displays 74% and 87% sequence identity with the coding regions of human and mouse IL-13 cDNA, respectively. The deduced amino acid sequence of rat IL-13 reveals 63% and 79% homology with the human and mouse proteins, respectively. Using the rat IL-13 cDNA as a molecular probe, increased production of IL-13 mRNA in renal and splenic tissue is demonstrated in the first 48 hours of antibody-induced glomerulonephritis in the rat. The data suggest a role for IL-13 in the inflammatory response in vivo.